Diseases of the cardiovascular system affect millions of people each year and are a leading cause of death in the United States and throughout the world. The costs to society from such diseases is enormous both in terms of the lives lost and in terms of the cost of treating patients through surgery. A particularly deadly form of heart disease which afflicts an estimated 3 million Americans is Congestive Heart Failure (CHF). Congestive heart failure is a syndrome caused by a failing heart, with congestion in the pulmonary or systemic circulation or both. It afflicts males more often than females, blacks more often than whites, and the elderly more often than younger persons. It is one of the most frequent causes of hospitalization of people aged 65 and older. Despite improvements in the management of patients with CHF, there appears to be no decline in mortality, presumably because of the aging of the population and the improved survival of patients with predisposing conditions, such as chronic ischemic heart disease.
The most common cause of congestive failure is coronary artery diseasexe2x80x94narrowing of the arteries supplying blood to the heart muscle. Although coronary disease often starts at an early age, congestive failure occurs most often in the elderly. Among people more than 70 years old, about 8 out of 1,000 are diagnosed with congestive heart failure each year. The majority of these patients are women, probably because men are more likely to die from coronary artery disease before it progresses to heart failure.
Heart failure is also associated with untreated hypertension, alcohol abuse, and drug abuse (primarily cocaine and amphetamines) at any age. Hyperthyroidism and various abnormalities of the heart valves (particularly aortic and mitral) are among the other disorders that can cause heart failure. In addition, viral infection or inflammation of the heart (myocarditis) or primary heart muscle disease (cardiomyopathy), and in rare instances, extreme vitamin deficiencies, can result in heart failure.
Heart failure may occur suddenly, or it may develop gradually. When heart function deteriorates over years, one or more conditions may exist. The strength of muscle contractions may be reduced, and the ability of the heart chambers to fill with blood may be limited by mechanical problems, resulting in less blood to pump out to tissues in the body. Conversely, the pumping chambers may enlarge and fill with too much blood when the heart muscle is not strong enough to pump out all the blood it receives. In addition, as the architecture of the heart changes as it enlarges, regurgitation of the mitral valve may develop, making the heart failure even worse. An enlarged heart, called cardiomyopathy, is a particularly debilitating form of heart disease which effects as many as 40% of patients with congestive heart failure.
Traditional therapeutic techniques for the treatment of congestive heart failure have been less than completely effective for a majority of patients treated. Drug therapy is one of the most widely used means of reducing the debilitating effects of CHF and for improving the quality of life of patients. Diuretics are often prescribed to help the kidneys eliminate excess water and sodium, thereby reducing the blood volume and the heart""s workload. Digitalis may be prescribed to increase the heart""s pumping action and increase the work done by the heart. Vasodilators, including angiotensin converting enzyme (ACE) inhibitors, may be used, along with diuretics, in patients with mild-to-moderate or severe congestive failure. ACE inhibitors, which include captopril (Capoten) and enalapril (Vasotec), block the production of a substance called angiotensin II, a potent constrictor of blood vessels. By causing the dilation of blood vessels, vasodilators decrease the amount of work that must be done by the heart as the blood pressure of the patient is decreased with increased vessel diameter. Nitrates and glycosides are also widely utilized in the treatment of heart failure to improve cardiac function and decrease symptoms.
Drug therapy has proved to be ineffective in completely treating more severe forms of CHF. Although ACE inhibitors and newer drug combinations have provided some relief for many patients, drugs often do not attack the root of the problem: a weak heart. Although workload on the heart is decreased through drug therapy, the pumping action of the heart is generally not improved long term in the case of most drugs. Also, in the case of drugs like digitalis, nitrates and glycosides, researchers remain unsure as to the long term debilitating affects that these drugs may have on an already weakened heart. Many believe that enhancement of the heart""s performance through drug therapy further damages the weakened muscles of the heart in the long term. Drug therapy may also be less than desirable for patients who suffer from moderate to severe side effects. For example, the use of ACE inhibitors often is accompanied by a persistent cough. Angioedema is another potential side effect of ACE inhibitors which can be potentially life threatening. Diuretics may dangerously decrease the body""s supply of potassium and other important vitamins and require additional corrective measures to maintain proper body chemistry. Finally, drug therapy often results in only short term gains to the patient. Although short term mortality of patients may be reduced in patients using aggressive drug therapy, after 3 to 5 years, drugs often offer little reduction in the rate of mortality for CHF patients.
Surgical intervention is another means for improving the condition of weakened hearts. When heart failure is due to valvular disease, the patient may have surgical implantation of an artificial heart valve or valve repair to help increase cardiac function. Surgery may also be helpful in correcting congenital heart defects that can lead to heart failure. Coronary artery bypass graft surgery or catheterization using balloon angioplasty are among the therapeutic techniques used to prevent and treat heart failure caused by occluded, or blocked, arteries. Additionally, newer techniques for myocardial revascularization and improved cardiac functioning include transmyocardial laser revascularization, implantation of mechanical assist devices, implantable cardioverters/defibrillators and dynamic cardiomyoplasty.
Implantation of permanent or temporary mechanical assist devices is one method by which ventricular function can be augmented in a diseased heart. A number of devices and methods are known in the art for compensating mechanically for the reduced ventricular output. Such devices include rotary blood flow pumps, intraaortic balloon pumps, axial flow pumps, external mechanical assist devices, and centrifugal blood flow pumps. The pump devices are traditionally used to augment the functioning of the left or right side of the heart by removing blood from one portion of the heart into a downstream portion of the patient""s vasculature. For example, for ventricular xe2x80x9cunloadingxe2x80x9d of the left heart, an axial flow pump may be inserted into the left ventricle via the aortic arch of the patient. The pump will remove blood from the ventricle and pump it into the aortic arch where it will flow normally to the remainder of the patient""s arterial system. Right heart unloading is similarly accomplished except that blood is typically removed from the right atrium or ventricle and pumped into the pulmonary artery. In contrast, external ventricular assist devices are generally surgically attached to the external surface of the heart and compress the ventricle of the heart during contraction so as to augment the contraction and improve cardiac output.
Mechanically assisting the functioning of the heart often presents substantial practical problems which prevent this method of CHF treatment from being the most desirable therapeutic option. Mechanical assist devices are often very expensive and difficult to install. Devices which have components external to the patient can detract significantly from the quality of life of the patient. Installation of the device may also lead to infection or rejection of the device by the patient""s immune system. Thrombosis is also a potential complication caused by foreign bodies within the patient""s bloodstream. The potential for thrombosis often requires aggressive anticoagulant therapy to prevent embolic material from forming in the bloodstream and causing serious physiological consequences. Mortality is also still high in those patients who have a cardiac assist device installed. Because of the high incidence of complications with cardiac assist devices, patients are often weaned from the device after the heart has been given a chance to rest and recover during a period of ventricular unloading. The hope is that the ventricular output will improve to a point that the patient may function without the device. Cardiac assist devices may also be used as a bridge to cardiac transplantation to support a patient with a failed heart while a suitable donor heart is being located for the patient.
Cardiac transplantation is another technique for treating heart disease. Cardiac transplantation is usually viewed as the last option for a patient with end-stage (terminal) heart disease. Unfortunately, for most patients suffering from congestive heart failure, cardiac transplantation may be the only currently available therapeutic option. As the name suggests, cardiac transplantation is a procedure wherein a healthy heart is taken from a donor cadaver and used to replace the diseased heart of the patient. Transplantation is accompanied by many risk factors which contribute to a high incidence of failed procedures and undesirability as a therapeutic option. These risk factors include the age of the patients, a decreasing number of donors, the extremely high cost of the procedure, high mortality on the waiting list, high morbidity under immunosuppressive therapy and problems with graft vasculopathy. Because of the high mortality of the procedure, cardiac transplantation is considered a last resort for treating CHF.
Spurred by the complications associated with existing therapeutic options for treating dilated cardiomyopathy (an enlarged heart), surgeons have experimented with a method by which the ventricle of the heart is reduced in size to more approximate the heart""s normal architecture. Called ventricular remodeling, the procedure requires the surgeon to remove a golf-ball size piece of tissue from the ventricle wall and then reshape the heart into a more efficient pumping machine. The procedure is usually accompanied by repair or replacement of any leaky or malfunctioning heart valves and those damaged or destroyed by the remodeling itself. One of the complications of dilated cardiomyopathy is that a considerable amount of xe2x80x9cdead spacexe2x80x9d exists within the enlarged ventricle which is not expelled during the contraction of the weakened heart, thus reducing the efficiency of the heart. Ventricular remodeling reduces the size of the diseased ventricle and eliminates the xe2x80x9cdead spacexe2x80x9d within the ventricle, resulting in an overall increase in the efficiency of the heart.
Due to the high incidence of complications of ventricular remodeling, it is not always the most desirable means of treating CHF. The procedure fails in approximately 1 in 4 patients undergoing the procedure. These patients must then be supported by a mechanical support device as described above or must undergo an immediate heart transplant procedure to survive. The procedure is also only effective for correcting decreased cardiac functioning resulting from dilated cardiomyopathy. Approximately 60% of CHF patients who are in need of a heart transplant to survive do not have an enlarged heart and would not be aided by the procedure.
From the foregoing it can be seen that CHF is a particularly deadly disease which affects millions of Americans every year. Traditional therapeutic techniques have also proven less than completely effective with most forms of CHF. Drug therapies, implantable devices, and currently known surgical procedures have a number of associated complications and risks which can prove potentially deadly to the patient.
Thus, it would be desirable to have devices and techniques which increase the cardiac output of a diseased heart without the associated complications and risks of known devices and techniques. Such devices should be simply and easily installed with a minimum of trauma to the patient, and preferably, would be capable of installation using minimally invasive surgical techniques. Use of the device should also be possible without the need to put the patient through the trauma of a xe2x80x9cstopped heartxe2x80x9d operation supported by cardiopulmonary bypass. The devices and techniques would preferably be employed as a permanent means of cardiac augmentation or, alternatively, as a temporary means of improving cardiac performance while awaiting a heart transplant.
A preferred device of the present invention comprises a ventricular assist device for increasing the ventricular output of the heart without providing external mechanical assistance to the heart, the device comprising a reinforcing portion operably engaging a portion of the heart tissue wherein the reinforcing portion is configured to restrict the motion of the portion of the heart tissue. The reinforcing portion is configured so that the heart tissue is prevented from expanding fully where the tissue is engaged by the reinforcing portion. A number of means exist for creating the reinforcing portion of the device. In one preferred embodiment, the reinforcing portion comprises a plurality of pursestring sutures installed in the portion of the heart tissue to be restricted, wherein the placement of the pursestring sutures defines the portion of the heart tissue to be restrained.
In another embodiment, the reinforcing portion comprises a patch of material installed in facing engagement to the portion of the heart tissue to be restrained. A number of materials are suitable for this application, including nylon, plastic, silicone, stainless steel, polyester fabric, pericardial tissue (either human, bovine, or porcine tissue), and other biocompatible biologic material. The material may be fixed in facing engagement to the portion of the heart tissue to be restrained using a plurality of sutures. Staples, tissue adhesive, rivets, and other standard surgical fastening techniques may also be used to fix the reinforcing material to the surface of the heart.
In another embodiment of the device of the present invention, the reinforcing portion comprises a pad assembly engaging the portion of heart to be restrained. The pad assembly is preferably configured to reduce the ventricular expansion of the portion of the heart to be restrained. The pad assembly may be held in engagement with the surface of the heart by a frame made from a number of members which encircle the heart and hold the pad assembly firmly against the portion of the heart to be restrained. The pad assembly may also be held in place by a harness made from highly flexible straps of biocompatible material, wherein the harness encircles around the heart to hold the pad assembly firmly against the portion of the heart tissue to be restrained.
In another embodiment of the present invention, the pad assembly is held in engagement with the portion of the heart tissue to be restrained with an anchor member. The anchor member is preferably stainless steel or other biocompatible material such as polypropylene or nylon, which is fastened at one end to the surface of the heart to be restrained. The second end of the anchor member is configured to be anchored to a relatively fixed structure in relation to the portion of the heart to be restrained. In one embodiment of the device of the present invention, the second end of the anchor member is configured to be fixed to a rib of a patient. Alternatively, the sternum bone or other suitable skeletal structure may be used to fix the motion of the portion of the heart to be restrained. It is only important that the portion of the heart to be restrained be fixed in relation to the remainder of the heart during expansion of the heart. In one embodiment of the present invention, the second end of the anchor member is configured to be fixed to a wall of the heart opposite the portion of the heart to be restrained. The anchor portion is thus installed inside the ventricle or atrium of the heart and restrains a portion of the heart wall by fixing the portion of the heart to be restrained to an opposite wall of the heart, such as a septal wall.
In a preferred embodiment, the reinforcing portion comprises an annular ring engaging the portion of the heart to be restrained. The ring may be sewn to the portion of the heart to be restrained, or it may be fixed using staples, surgical adhesive, or other traditional surgical fastening methods, or it may be held in engagement with the portion of the heart to be restrained using a harness or frame made from flexible straps or members as previously described.
In another embodiment of the present invention, the reinforcing portion comprises two or more motion restricting pads which are sutured, stapled, or otherwise fastened to the surface of the heart and then conjoined using one or more straps or tethers. The straps may be adjusted to pull the pads closer in relation to each other and thus reduce the motion of the heart wall between the two or more reinforcing pads.
The methods of the present invention for passively assisting cardiac performance generally comprise the steps of (1) providing a site of surgical access to the portion of the heart to be restrained; and (2) reducing the ventricular movement of the portion of the heart to be restrained. In one method of the present method, the step of reducing the ventricular movement of the portion of the heart to be restrained comprises installing a plurality of sutures in the portion of the heart to be restrained. In another method, the step of reducing the ventricular movement of the portion of the heart to be restrained comprises installing a patch of reinforcing material in facing engagement with the portion of the heart to be restrained. The patch may be installed using sutures, staples, surgical adhesive, and other surgical fastening techniques. Yet in another method, the step of reducing the ventricular movement of the portion of the heart to be restrained comprises fixing a portion of the pericardium of a patient or from a donor to the portion of the heart to be restrained. In an alternative method of the present invention, the step of reducing the ventricular movement of the portion of the heart to be restrained comprises fixing the portion of the heart to be restrained to a body structure which is relatively fixed in relation to the portion of the heart to be restrained. The body structure may be the patients ribs, sternum, or wall of the heart opposite the portion to be restrained.
Additional steps of the methods of the present invention may include the step of closing the site of surgical access. The method of the present invention may also be practiced on a patient who is supported by cardiopulmonary bypass (CPB) prior to reducing the ventricular movement of the portion of the heart to be restrained. Preferably, however, the methods of the present invention will be practiced in a minimally invasive manner and on a beating heart.
Another embodiment of the present invention is device for displacing a volume of a portion of a diseased heart comprising an expandable member configured to fit into a chamber of the diseased heart and reduce the available blood volume of the chamber of the heart; and an inflation portion. A method of using the volume displacement device of the present invention includes installing a ventricular displacement device comprising an inflation portion and an expandable member into the chamber of the heart, and expanding the expandable member to displace a portion of the blood volume of the chamber of the heart.
Alternatively, the volume of a chamber may be reduced using the teachings of the present invention by making an incision through the pericardium and myocardium of the left ventricle, repairing the incision in the pericardium; pushing the pericardium into the ventricle through the incision in the myocardium to form a pericardial sack in the left ventricle; providing inflation fluid to the pericardial sack to fill the pericardial sack and displace a portion of the blood volume of the ventricle; and closing the incision in the myocardium to close surgical access to the ventricle and to seal the inflation fluid in the pericardial sack.